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POLYCYTHÆMIA AND IRON DEFICIENCY IN PULMONARY " EMPHYSEMA "
915
opinion, therefore, the analysis of acid-base status is an important means of improving diagnosis and therapy of hypertrophic pyloric stenosis in infants. In
our
University Children’s Hospital, Würzburg, Germany.
J. STRÖDER H. BLENNEMANN.
POLYCYTHÆMIA AND IRON DEFICIENCY IN PULMONARY " EMPHYSEMA " SIR,-In our experience,12chronic bronchitis may be the primary cause of inadequate erythrocyte response to the low arterial-oxygen saturation in patients with pulmonary emphysema such as those described by Dr. Fielding and Dr. Zorab (Aug. 8). In a group of 15 patients investigated by iron kinetic studies and determinations of arterial-oxygen saturation, 10 presented a clinical and bacteriological picture of bronchial infection. Results suggested that haemoglobin synthesis was inhibited by the infection. In fact, the only 3 patients with emphysema and polycythxmia were the patients without bronchial infection. I believe that the cause of the " apparent " latent iron deficiency which Dr. Fielding and Dr." Zorab found is the infection. I should like to emphasise apparent ", because these patients have normal or low values for serum-iron with increased iron storage. We have recently treated patients with chronic pulmonary emphysema and low serum-iron values with desferrioxamine and have found higher than normal levels of iron in their urine. These results confirm the iron overload in these patients. The erythrocyte response to the iron therapy in some of the patients of Dr. Fielding and Dr. Zorab cannot be regarded as evidence of iron deficiency for two reasons: first, the controls of erythrocyte volume and haemoglobin mass were carried out 8-10 weeks after iron treatment had begun and, in this time, the infection might have resolved (unfortunately Dr. Fielding and Dr. Zorab do not say whether their patients were treated with antibiotics during the interval); and, secondly, we have occasionally found an increase of serum-iron levels and erythrocyte mass after a large dose of iron in patients with chronic infections.3 Finally, in rats we produced experimental emphysema with constant increase of erythrocyte volume.4 In my opinion this result means that low arterial oxygen saturation increases erythrocyte production in patients with pulmonary emphysema as well as in people living at
high altitudes; but, when recurrent bronchial infections are present, haemoglobin synthesis diminishes and becomes manifest as an inadequate erythrocyte response to the hypoxia. Institute of Medical Pathology of the University of Bologna,
Bologna, Italy.
SANTE TURA.
BACK-PRESSURE SIR,-By a loose phrase I mean one which, though it may be in everyday use, has never been precisely defined. Indeed, it may ordinarily be used in a sense in which it is not susceptible to accurate definition at all. " Back-
pressure " is such
a
phrase.
a thing as back-pressure. It might be pulse or wave of pressure, propagated backwards against a sufficiently slowly moving stream of fluid, such as probably happens at the start of cardiac systole. But this is not what is usually meant by the expression. Instead, " backpressure " is used to describe the increase of venous pressure in
Of course, there is such
defined
as a
heart-failure. It is still even taught that venous pressure increases because the heart ceases to clear the blood away as fast as it is entering the veins. 1. 2.
Tura, S., Poeycove, M., Gelpi, A. P. J. Nucl. Med. 1962, 3, 110. Campanacci, D., Bonomini, V., Butturini, U., Gunella, G., Magnani, B., Pieragnoli, E., Telo, W., Tura, S. Relazione 60° Congresso Società
3.
Campanacci, D., Tura, S., Daineli, G. Relazione 19° Congresso Nazionale Società Italiana Ematologis; p. 317. 1963. Tura, S. Proc. Soc. exp. Biol., N.Y. 1960, 103, 713.
Italiana Medicina Interna. Roma 1959.
4.
This is surely nonsense; for the output of a failing heart declines as least at the same rate as the heart fails to withdraw blood from the veins. This implies that the arrival of blood in the veins is reduced pari passu with decrease in the rate of its withdrawal. I say " at least " for the gradual increase in size of the failing heart implies that its intake declines infinitesimally more slowly than its output. Because the blood-vessels are a system of elastic tubes, the whole of the blood is in a state of compression, like the contents of an inflated balloon. If it were possible to stop the heart without altering the calibre of any of the blood-vessels, arterial and venous pressure would become equal just midway between their previous levels. After death, because of the loss of vasomotor tone, the levels become equal below the midpoint, though above venous pressure in life. For simple mechanical reasons, the poorer the cardiac output or the larger the total calibre of the arterioles, the nearer arterial and venous pressure tend to approach each other and the basic pressure or overall vascular compression. Sometimes in heartfailure, arterial pressure falls as venous pressure rises. Sometimes arterial pressure is maintained, and there must then have been a simultaneous rise in overall vascular compression, due either to increased blood-volume or to increased vascular
(probably largely venous)
tone.
Students tell me that they find this explanation much easier to grasp than that presented to them in textbooks. Is there any purpose in retaining the muddle-headed con" " cept of back-pressure or the equally indefinable and " unmeasurable venous return " ? H. DAINTREE JOHNSON. London, W.1.
Obituary CUTHBERT ALFRED BOZMAN
O.B.E., M.B. Edin., D.P.H. THE death of Colonel Bozman on Oct. 10 at the age of 65 years, while on holiday in the Lake District, ends a career in hygiene and public health which has had an influence in three continents. He was the son of an Irish father, and after service in the 1914-18 war in the Infantry and the R.A.F. he graduated M.B. from the University of Edinburgh in 1924. The following year he joined the Indian Medical Service, and he was posted to the Andaman Islands, where his interest in epidemiology was aroused by the occurrence of a severe form of epidemic jaundice, later shown to be Weil’s disease. After taking the D.P.H. in 1931, he served in several military districts as a laboratory specialist and as D.A.D. PATH. In 1933 he was transferred to civil employment and he spent some years in Burma as assistant director, and later director, of public health. He lectured on hygiene at the Rangoon Medical College and for a time qcted as director of the Harcourt Butler Institute of Public Health. Early in 1938 Bozman opted to return to India, from which Burma had become detached by constitutional rearrangement, and he was posted to Bombay as port health officer. From Bombay he was called to Delhi to join the staff of the director-general of the I.M.S. Later he became a public health commissioner with the Government of India. He was appointed o.B.E. in 1946. In the same year he took premature leave, pending retirement, to join the epidemiological section of the Ministry of Health in London; but he did not remain there long. For family reasons he left London for Dundee as lecturer in public health at the University of St. Andrews, and later he moved to the milder climate of Cornwall. But he was soon back at work, for the Foreign Office appointed him as successor to Sir Eric Pridie in the British Middle East Bureau with headquarters in Cairo. When Bozman’s appointment there ended, he went to Uganda as professor of public health at Makerere. In 1956
opinion, therefore, the analysis of acid-base status is an important means of improving diagnosis and therapy of hypertrophic pyloric stenosis in infants. In
our
University Children’s Hospital, Würzburg, Germany.
J. STRÖDER H. BLENNEMANN.
POLYCYTHÆMIA AND IRON DEFICIENCY IN PULMONARY " EMPHYSEMA " SIR,-In our experience,12chronic bronchitis may be the primary cause of inadequate erythrocyte response to the low arterial-oxygen saturation in patients with pulmonary emphysema such as those described by Dr. Fielding and Dr. Zorab (Aug. 8). In a group of 15 patients investigated by iron kinetic studies and determinations of arterial-oxygen saturation, 10 presented a clinical and bacteriological picture of bronchial infection. Results suggested that haemoglobin synthesis was inhibited by the infection. In fact, the only 3 patients with emphysema and polycythxmia were the patients without bronchial infection. I believe that the cause of the " apparent " latent iron deficiency which Dr. Fielding and Dr." Zorab found is the infection. I should like to emphasise apparent ", because these patients have normal or low values for serum-iron with increased iron storage. We have recently treated patients with chronic pulmonary emphysema and low serum-iron values with desferrioxamine and have found higher than normal levels of iron in their urine. These results confirm the iron overload in these patients. The erythrocyte response to the iron therapy in some of the patients of Dr. Fielding and Dr. Zorab cannot be regarded as evidence of iron deficiency for two reasons: first, the controls of erythrocyte volume and haemoglobin mass were carried out 8-10 weeks after iron treatment had begun and, in this time, the infection might have resolved (unfortunately Dr. Fielding and Dr. Zorab do not say whether their patients were treated with antibiotics during the interval); and, secondly, we have occasionally found an increase of serum-iron levels and erythrocyte mass after a large dose of iron in patients with chronic infections.3 Finally, in rats we produced experimental emphysema with constant increase of erythrocyte volume.4 In my opinion this result means that low arterial oxygen saturation increases erythrocyte production in patients with pulmonary emphysema as well as in people living at
high altitudes; but, when recurrent bronchial infections are present, haemoglobin synthesis diminishes and becomes manifest as an inadequate erythrocyte response to the hypoxia. Institute of Medical Pathology of the University of Bologna,
Bologna, Italy.
SANTE TURA.
BACK-PRESSURE SIR,-By a loose phrase I mean one which, though it may be in everyday use, has never been precisely defined. Indeed, it may ordinarily be used in a sense in which it is not susceptible to accurate definition at all. " Back-
pressure " is such
a
phrase.
a thing as back-pressure. It might be pulse or wave of pressure, propagated backwards against a sufficiently slowly moving stream of fluid, such as probably happens at the start of cardiac systole. But this is not what is usually meant by the expression. Instead, " backpressure " is used to describe the increase of venous pressure in
Of course, there is such
defined
as a
heart-failure. It is still even taught that venous pressure increases because the heart ceases to clear the blood away as fast as it is entering the veins. 1. 2.
Tura, S., Poeycove, M., Gelpi, A. P. J. Nucl. Med. 1962, 3, 110. Campanacci, D., Bonomini, V., Butturini, U., Gunella, G., Magnani, B., Pieragnoli, E., Telo, W., Tura, S. Relazione 60° Congresso Società
3.
Campanacci, D., Tura, S., Daineli, G. Relazione 19° Congresso Nazionale Società Italiana Ematologis; p. 317. 1963. Tura, S. Proc. Soc. exp. Biol., N.Y. 1960, 103, 713.
Italiana Medicina Interna. Roma 1959.
4.
This is surely nonsense; for the output of a failing heart declines as least at the same rate as the heart fails to withdraw blood from the veins. This implies that the arrival of blood in the veins is reduced pari passu with decrease in the rate of its withdrawal. I say " at least " for the gradual increase in size of the failing heart implies that its intake declines infinitesimally more slowly than its output. Because the blood-vessels are a system of elastic tubes, the whole of the blood is in a state of compression, like the contents of an inflated balloon. If it were possible to stop the heart without altering the calibre of any of the blood-vessels, arterial and venous pressure would become equal just midway between their previous levels. After death, because of the loss of vasomotor tone, the levels become equal below the midpoint, though above venous pressure in life. For simple mechanical reasons, the poorer the cardiac output or the larger the total calibre of the arterioles, the nearer arterial and venous pressure tend to approach each other and the basic pressure or overall vascular compression. Sometimes in heartfailure, arterial pressure falls as venous pressure rises. Sometimes arterial pressure is maintained, and there must then have been a simultaneous rise in overall vascular compression, due either to increased blood-volume or to increased vascular
(probably largely venous)
tone.
Students tell me that they find this explanation much easier to grasp than that presented to them in textbooks. Is there any purpose in retaining the muddle-headed con" " cept of back-pressure or the equally indefinable and " unmeasurable venous return " ? H. DAINTREE JOHNSON. London, W.1.
Obituary CUTHBERT ALFRED BOZMAN
O.B.E., M.B. Edin., D.P.H. THE death of Colonel Bozman on Oct. 10 at the age of 65 years, while on holiday in the Lake District, ends a career in hygiene and public health which has had an influence in three continents. He was the son of an Irish father, and after service in the 1914-18 war in the Infantry and the R.A.F. he graduated M.B. from the University of Edinburgh in 1924. The following year he joined the Indian Medical Service, and he was posted to the Andaman Islands, where his interest in epidemiology was aroused by the occurrence of a severe form of epidemic jaundice, later shown to be Weil’s disease. After taking the D.P.H. in 1931, he served in several military districts as a laboratory specialist and as D.A.D. PATH. In 1933 he was transferred to civil employment and he spent some years in Burma as assistant director, and later director, of public health. He lectured on hygiene at the Rangoon Medical College and for a time qcted as director of the Harcourt Butler Institute of Public Health. Early in 1938 Bozman opted to return to India, from which Burma had become detached by constitutional rearrangement, and he was posted to Bombay as port health officer. From Bombay he was called to Delhi to join the staff of the director-general of the I.M.S. Later he became a public health commissioner with the Government of India. He was appointed o.B.E. in 1946. In the same year he took premature leave, pending retirement, to join the epidemiological section of the Ministry of Health in London; but he did not remain there long. For family reasons he left London for Dundee as lecturer in public health at the University of St. Andrews, and later he moved to the milder climate of Cornwall. But he was soon back at work, for the Foreign Office appointed him as successor to Sir Eric Pridie in the British Middle East Bureau with headquarters in Cairo. When Bozman’s appointment there ended, he went to Uganda as professor of public health at Makerere. In 1956